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CVPR > CVPR Week 8: Renal diseases Part B > Flashcards

CVPR Week 8: Renal diseases Part B Flashcards

1
Q

SLE AKA

A

Systemic lupus erythematosus

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2
Q

SLE pathology

A

auto-immune disease

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3
Q

SLE is most common in?

A
  • Women
  • and is 2-3 times more common in black and hispanic populations
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4
Q

SLE clinical consistency

A

clinically very heterogenous

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5
Q

SLE organ systems affected

A

affects multiple organ systems and is a multi-system disease

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6
Q

SLE hallmark

A
  • auto-antibodies
  • ANA, anti-double stranded DNA, anti-Smith antibody
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7
Q

SLE diagnostic criteria

A
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8
Q

SLE skin findings

A

Malar Rash

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9
Q

Lupus nephritis

A
  • Renal disease causes significant morbidity and mortality
  • Glomerulonephritis WHO classes I-VI
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10
Q

Lupus nephritis pathology

A
  • Caused by immune complex deposits (deposits may cause GBM duplication called “tram-tracking”
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11
Q

Lupus nephritis immunofluorescence microscopy

A

staining for IgG, IgA, IgM, C3, C1q (=full house)

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12
Q

Lupus nephritis full house

A
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13
Q

Classifications of Lupus Nephritis

A
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14
Q

Class I Lupus nephritis

A

minimal or no abnormality

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15
Q

Class II Lupus nephritis

A

mesangial GN

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16
Q

Class III Lupus nephritis

A

Focal proliferative GN

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17
Q

Class IV Lupus nephritis

A

diffuse proliferative GN (most common)

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18
Q

Class V Lupus nephritis

A

membranous lupus nephritis

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19
Q

Class VI Lupus nephritis

A

chronic with glomerular scarring

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20
Q

Identify

A
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21
Q

Identify

A
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22
Q

Identify

A
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23
Q

Identify

A
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24
Q

What is Amyloidosis?

A
  • A group of systemic diseases defined by deposits of extracellular fibrillar proteins
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25
Q

Amyloidosis pathology

A

Deposits of extracellular fibrillar proteins

  • deposits cause tissue damage and impair organ function
  • Deposits are of abnormal misfolded proteins that normally would be degraded by macrophages
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26
Q

Amyloidosis is associated with?

A

neoplastic, inflammatory and inherited disorders

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27
Q

Amyloid definition

A
  • Amyloid is a broad term encompassing > 20 different proteins that can form abnormal fibrils
  • Fibrils with beta-pleated sheet conformation
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28
Q

How are amyloid fibrils arranged

A

in beta-pleated sheets

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29
Q

Most common forms of systemic amyloidosis

A
  • Amyloid light chain
  • Amyloid-associated
30
Q

AL protein AKA

A

Amyloid light chain

31
Q

AA type protein AKA

A

Amyloid-associated

32
Q

Identify

A
33
Q

Identify

A
34
Q

Identify

A
35
Q

Renal amyloidosis light microscopy

A
  • Amyloid deposited in glomerulus
  • widening of mesangial matrix and GBM
  • Obliterates capillary lumens
  • Deposits in arteries, arterioles, peritubular (deposits are extracellular)
36
Q

Describe amyloid deposits

A

amyloid deposits begin between cells, encroaches on them

Pink (or red) color on routine histology, like melted strawberry ice cream

37
Q

Renal amyloidosis special stain

A

Congo red dye

38
Q

Renal amyloidosis as seen with Congo red dye

A
  • Orange or red color
  • apple-green birefringence under polarized light
  • reflects crossed beta-pleated configuration of amyloid fibrils
39
Q

Renal amyloidosis electron microscopy features

A
  • Thin unoriented non-branching fibrins
40
Q

Renal involvement in diabetes

A

Renal failure is the 2nd most common cause of death in diabetes (after myocardial infarction)

41
Q

The key pathogenic factor for renal damage in diabetes

A
  • formation of advanced glycation end products
  • non-enzymatic glycosylation of basement membranes
42
Q

Renal pathology in diabetes

A
  • Glomerular lesions
    • capillary basement membrane thickening
    • diffuse glomerulosclerosis
    • Nodular glomerulosclerosis Kimmelstiel-Wilson
    • Pyelonephritis
  • Renal arteriolosclerosis (hyalinosis) and atherosclerosis
  • Pyelonephritis
    • including papillary necrosis
43
Q

Identify

A
44
Q

Identify

A
45
Q

Identify

A
46
Q

Identify

A
47
Q

Identify

A
48
Q

Identify

A
49
Q

Prevalence of Acute Pyelonephritis

A

Very common, it is one of the most common kidney diseases

50
Q

Acute pyelonephritis etiology

A
  • Ascending from urethra and bladder, typically from patient’s own fecal flora
  • gram-negative bacilli
    • E. Coli
    • Proteus
    • Klebsiella
    • Streptococcus faecalis
51
Q

Acute pyelonephritis risk factors

A
  • Obstruction: stones, tumors, enlarged prostate, pregnancy
  • bladder dysfunction (e.g. spinal cord injury, diabetes)
  • Vesico-ureteral reflux - due to incompetent vesico-ureteral valve

leading to decreased urine flow

52
Q

Acute pyelonephritis features of light microscopy

A
  • Acute inflammatory cells in tubules, interstitium, kidney pelvis, bladder and urine
  • white cell casts
  • Edema
  • Abscess formation
  • Tubular necrosis in severe cases
53
Q

Acute pyelonephritis features on urinalysis

A
  • Neutrophils in the urine
  • White cell casts in the urine
54
Q

Identify

A
55
Q

Identify

A
56
Q

Identify

A
57
Q

Acute pyelonephritis complications

A
58
Q

Identify

A
59
Q

Identify

A
60
Q

Identify features and disease processes involved

A

In the context of Acute pyelonephritis

61
Q

Identify features and disease processes involved

A

In the context of Acute pyelonephritis

62
Q

Acute pyelonephritis can evolve?

A

Chronic pyelonephritis

which is the evolution into chronic inflammation with scarring

63
Q

Describe chronic pyelonephritis

A
  • When acute pyelonephritis evolves into chronic inflammation with scarring called chronic pyelonephritis
  • Polar scars with blunted calices
  • Tubular atrophy, chronic lymphocytic infiltrate and interstitial fibrosis
64
Q

Drug-induced interstitial nephritis etiology

A
65
Q

Drug-induced interstitial nephritis clinical features

A
  • fever
  • blood eosinophilia
  • rash
  • hematuria
  • mild-proteinuria
  • leukocyturia with eosinophils
  • increased serum creatinine or acute renal failure
66
Q

Drug-induced interstitial nephritis pathogenesis

A

abnormal immune reaction

67
Q

Type I Drug-induced interstitial nephritis

A
  • acute hypersensitivity (type I hypersensitivity reaction)
  • The drug binds to proteins in tubular cells and becomes immunogenic (i.e. functions as hapten)
  • Idiosyncratic, i.e. NOT dose-related
68
Q

Type IV Drug-induced interstitial nephritis

A
  • When granulomas present (less common than type I)
  • Delayed-type hypersensitivity reaction (Type IV hypersensitivity reaction)
69
Q

Identify

A
70
Q

Identify

A
71
Q

Drug-induced interstitial nephritis features under light microscopy

A
72
Q

Drug-induced interstitial nephritis clinical course

A

CVPR (93 decks)

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